Outline

Objective

Dural arteriovenous fistulas (dAVFs) appear to be acquired lesions. The exact pathogenesis of dAVFs remains unclear, although sinus thrombosis and venous hypertension might be important factors for their formation. Earlier reports have shown that angiogenic growths factors may contribute to the development of dAVFs. Here we try to explore possible mechanisms of their pathogenesis by immunohistochemical investigation of various angiogenesis-related proteins.

Methods

We examined the expression of proteins related to proliferation (PCNA, MIB-1) and angiogenesis (bFGF, TGFα, VEGF and its receptors Flk-1 and Flt-1) as well as the hypoxia-inducible factor in surgical specimens in order to further investigate the role of hypoxia-induced angiogenesis for the pathogenesis of dAVFs.

Results

There was no positive immunostaining for MIB-1, but 3 out of 8 specimens showed a positive staining for PCNA. VEGF, Flk-1 and Flt-1 stained positively in 7, 2, and 5 of 7 specimens, respectively. Hif-1a stained positively in all available specimens.

Conclusions

DAVFs might be acquired dynamic vascular malformations with low proliferative activity. Local tissue hypoxia appears to be an important step of vasculogenesis during the formation of dAVFs.